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Prevalence and immuno-metabolic associations of
frailty in older Australian men living with HIV: a cross-sectional analysis
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from Jules....frailty in HIV+ men association with inflammation markets, mitochondrial dysfunction markers, and metabolic dystegulation .....neurotoxicity & mitochondrial toxicity is associated with many ARTs and frailty is likely associated with all this
CROI:Neurotoxicity Screening of Antiretroviral Drugs With Human iPSC-Derived Neurons
CROI:Frailty is associated with NNRTI-based Initial ART and Modifiable Risks in ACTG 5322 - (02/29/16)
CROI:Belly Fat (lipodystophy) May be Caused by Metabolic Abnormalities: immune activation/inflammation/senescence
CROI:Mitochondrial DNA Copy Number and Neurocognitive Impairment in HIV-Infected Persons....."mtDNA associated with worse cognitive outcomes".....both HIV & ART duration associated with mtDNA damage
Reported by Jules Levin
Durban 2016 July 18-22
Yeoh H1,2, Cherry C1,3, Cheng A1, Palmer C1,2 *, Hoy J1 *, Crowe S1,2 *
1 Department of Infectious Diseases, The Alfred and Monash University, Melbourne, Australia. 2 Centre for Biomedical Research, Burnet Institute,
Melbourne, Australia. 3 School of Physiology, University of the Witwatersrand, Johannesburg, South Africa. * these authors contributed equally to this work
IAC:Differences in health-related quality of life highlight the different emphases of three frailty instruments in older Australian men living with HIV ....13% had HCV coinfection - (08/04/16)
Abstract
Background: Frailty, a manifestation of physical and psycho-social vulnerability, is a condition of increasing concern as the HIV population ages. The definition of frailty is contentious and the pathophysiology is unknown. This study compared two commonly used frailty instruments, and identified biomarkers associated with frailty, in older Australian HIV+ men.
Methods: HIV+ men aged over 50-years, on ART for >6 months were enrolled between March and August 2015 in a Melbourne HIV referral centre. Frailty was assessed using the Frailty Phenotype (FP), and the Frailty Index (FI). Markers of immune activation (%CD38+DR+ T-cell subsets), metabolic dysregulation (Glut1+ mean fluorescence intensity (MFI) of T-cells) and mitochondrial dysfunction (DiOC6(3)+ MFI of monocytes) were measured by flow cytometry, and the inflammatory marker, sCD163, was measured by ELISA. Differences in co-variates between frail and non-frail groups using FP were tested using Kruskal-Wallis tests, and correlations with the FI using Spearman´s rho. Linear and logistic regression models were constructed.
Results: 84 HIV+ men completed both clinical and laboratory aspects of the study: median age 59 years; 95% Caucasian, 93% had undetectable viral load. Using the FP, 10% (n=8) were categorized as frail, 52% (n=44) pre-frail and 38% (n=32) robust. The median FI score was 0.13, (0.25 was the cut-off between frail and non-frail), with 23% (n=19) categorised as frail on the FI. HIV+ pre-frail and frail men (using the FP) had higher levels of inflammation than robust men (mean plasma sCD163 3.07 vs. 2.35 ng/ml, respectively, p=0.015), remaining significant on multivariable analysis. The FI correlated with markers of inflammation, metabolic dysregulation and mitochondrial dysfunction (plasma sCD163 (ρ=0.263, p=0.036), Glut-1 MFI and DiOC6(3) MFI on non-classical monocytes (ρ=0.246, p=0.049; ρ=-0.248, p=0.048 respectively) with Glut-1 and DiOC6(3) remaining significant in multivariable analysis. Neither the FP nor the FI were associated with T-cell immune activation.
Conclusions: Frailty in older HIV+ men on ART using both tools was correlated with inflammatory marker, sCD163. The Frailty Index was also associated with markers of metabolic dysregulation and mitochondrial dysfunction in the inflammatory non-classical monocytes. Our findings do not support an association between frailty and T-cell immune activation.
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